Non-Inflammatory Chronic Pelvic Pain Syndrome Can Be Caused by Bladder Neck Hypertrophy

Abstract

Purpose: Little is known about the etiology of the non-inflammatory Chronic Pelvic Pain Syndrome (CPPS, NIH category IIIb). We conducted this study to determine whether endoscopic and urodynamic evaluation provide objectively measurable parameters that may support the rationale of therapeutic strategies for patients who failed to respond to medical treatment of non-inflammatory CPPS.

Materials and Methods: The 48 patients included in this study fulfilled the NIH criteria for non-inflammatory chronic pelvic pain syndrome category IIIb. All patients had received multiple courses of antimicrobial and/or anti-inflammatory drugs, but suffered recurrent symptoms. An endoscopic and urodynamic evaluation was performed after any medical treatment had been discontinued for at least 6 weeks.

Results: At urethrocystoscopy, no patient had endoscopic evidence of obstruction due to urethral stricture, but 29 patients (60%) were found to have significant bladder neck hypertrophy. At urodynamic evaluation, these 29 patients had an increased detrusor opening pressure DOP (49 vs. 29 cmH₂O), an increased detrusor pressure at maximal flow P_det,Qmax (55 vs. 34 cmH₂O), a decreased maximal flow Q_max (10 vs. 17 ml/s) and an increased postvoid residual urine PVR (67 vs. 17 ml) when compared to the 19 patients with a normal appearing bladder neck. These differences were statistically significant (p<0.05). When assessed with the NIH Chronic Prostatitis Symptom Index (CPSI) the two groups showed no difference in the domains of pain and quality of life impact but urinary symptoms were significantly more pronounced in the presence of bladder neck alterations.

Conclusions: Patients with non-inflammatory CPPS who fail to respond to medical treatment with antibiotics and/or anti-inflammatory drugs may have morphological alterations in form of bladder neck hypertrophy. This can be suspected when urinary symptoms, residual urine and decreased Q_max are present. These can be assessed by non-invasive methods. Endoscopic and/or urodynamic evaluation seem to be justified in these patients in order to establish the diagnosis, consider α-adrenergic blockade and avoid unnecessary antibiotic treatment.

Introduction

Prostatitis is one of the most common entities encountered in urological practice. A US national survey of physician visits from 1990 to 1994 compiled almost 2 million office visits yearly where the diagnosis of prostatitis was made [1]. Only 5% to 10% of cases are known to have a bacterial etiology. In about 90% of cases the cause is unknown [2]. The most common form is the chronic abacterial prostatitis or type III prostatitis, according to the National Institutes of Health (NIH) prostatitis classification system called Chronic Pelvic Pain Syndrome (CPPS) [3]. Numerous studies on prostatitis syndromes have focussed on an infectious etiology suggesting that microorganisms may be important causative agents [4], [5], [6], [7]. However, many patients are not cured by antimicrobial therapy and both patients and physicians are often frustrated in dealing with this condition. Although antimicrobial treatment is recommended as first line approach in patients with inflammatory CPPS (NIH category IIIa), there are still few evidence-based recommendations on how to proceed in patients with the non-inflammatory syndrome (NIH category IIIb) [8] since characteristic objective findings are missing. It is a common belief that probably various mechanisms may lead to the development of symptoms in CPPS IIIb. The present study was conducted to determine if these patients have functional and/or anatomical alterations of the lower urinary tract which could constitute pathophysiological mechanisms of their disease.